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. 2015 May 29;22(8):1250–1259. doi: 10.1038/cdd.2015.67

Figure 4.

Figure 4

EBOV infection induces adaptive immune cell dysfunctions. (a) Antibodies production represents the best correlate of protection during EBOV infection. Two different forms of EBOV GP, soluble GP (sGP) and glycosylated-GP (GlycGP), are able to drive antibodies shielding and misdirection. (b) EBOV infection of DC results in a deregulated DC/T synapse, characterized by an effective MHC-peptide/TCR interaction (signal 1), in a high inflammatory microenvironment (deregulated signal 3) in the absence of co-stimulatory accessories molecules on DC surface (ineffective signal 2). The inappropriate DC/T-cell interaction induces T-cell apoptosis, avoids CD4 T-cell clonal expansion, thus blocking all CD4 T-cell helper functions such as CD8-mediated cytotoxicity and antibodies-production by B cells